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J Am Coll Cardiol, 2008; 51:1369-1374, doi:10.1016/j.jacc.2007.11.071 © 2008 by the American College of Cardiology Foundation |

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* Division of Cardiology, Veterans Affairs Medical Center, Minneapolis, Minnesota
Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota
Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
PERFUSE Core Laboratory and Data Coordinating Center, Harvard Medical School, Boston, Massachusetts
|| Hypertrophic Cardiomyopathy Center, Division of Cardiology, Tufts-New England Medical Center, Boston, Massachusetts.
Manuscript received August 2, 2007; revised manuscript received November 2, 2007, accepted November 26, 2007.
* Reprint requests and correspondence: Dr. A. Selcuk Adabag, Section of Cardiology (111 C), Veterans Affairs Medical Center, One Veterans Drive, Minneapolis, Minnesota 55417. (Email: adaba001{at}umn.edu).
Objectives: Our aim was to determine whether myocardial fibrosis, detected by cardiovascular magnetic resonance (CMR), represents an arrhythmogenic substrate in hypertrophic cardiomyopathy (HCM).
Background: Myocardial fibrosis is identified frequently in HCM; however, the clinical significance of this finding is uncertain.
Methods: We studied prevalence and frequency of tachyarrhythmias on 24-h ambulatory Holter electrocardiogram (ECG) with regard to delayed enhancement (DE) on contrast-enhanced CMR in 177 HCM patients (age 41 ± 16 yrs; 95% asymptomatic or mildly symptomatic).
Results: Premature ventricular contractions (PVCs), couplets, and nonsustained ventricular tachycardia (NSVT) were more common in patients with DE than those without DE (PVCs: 89% vs. 72%; couplets: 40% vs. 17%; NSVT: 28% vs. 4%; p < 0.0001 to 0.007). Patients with DE also had greater numbers of PVCs (202 ± 655 vs. 116 ± 435), couplets (1.9 ± 5 vs. 1.2 ± 10), and NSVT runs (0.4 ± 0.8 vs. 0.06 ± 0.4) than non-DE patients (all p < 0.0001); DE was an independent predictor of NSVT (relative risk 7.3, 95% confidence interval 2.6 to 20.4; p < 0.0001). However, extent (%) of DE was similar in patients with and without PVCs (8.2% vs. 9.1%; p = 0.93), couplets (8.5% vs. 8.4%; p = 0.99), or NSVT (8.3% vs. 8.5%; p = 0.35).
Conclusions: In this large HCM cohort with no or only mild symptoms, myocardial fibrosis detected by CMR was associated with greater likelihood and increased frequency of ventricular tachyarrhythmias (including NSVT) on ambulatory Holter ECG. Therefore, contrast-enhanced CMR identifies HCM patients with increased susceptibility to ventricular tachyarrhythmias.
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